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Aging augments mitochondrial suscept...

The University of Iowa.

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Aging augments mitochondrial susceptibility to environmental stress.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Aging augments mitochondrial susceptibility to environmental stress./
作者:	Haak, Jodie L.
面頁冊數:	103 p.
附註:	Adviser: Kevin C. Kregel.
Contained By:	Dissertation Abstracts International69-07B.
標題:	Biology, Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3323422
ISBN:	9780549749790

Aging augments mitochondrial susceptibility to environmental stress.
Haak, Jodie L.

Aging augments mitochondrial susceptibility to environmental stress. - 103 p.

Adviser: Kevin C. Kregel.

Thesis (Ph.D.)--The University of Iowa, 2008.

The pathophysiology of aging is accompanied by a decline in tolerance to environmental stress. While mitochondria are the primary suspects in the etiology of aging, little is known about their ability to tolerate pertubations to homoeostasis in aged organisms. To illuminate the role of mitochondria in the increased susceptibility to heat stress that is seen with aging, young (6 mo) and old (24 mo) Fischer 344 rats underwent a heat stress protocol known to elicit cellular damage that is exaggerated in aged rats. Two and 24 h after heat stress, rats were euthanized, their livers removed, and hepatic mitochondria isolated. Electron microscopy and immunoblot analysis revealed extensive structural and morphological damage to mitochondria from young and, to a greater extent, old rats. Electron paramagnetic resonance spectrometry measurements of superoxide suggested that mitochondrial integrity is also altered during heat stress. After encountering a harmful perturbation such as heat stress, the mitochondrial stress response functions to correct damage that has occurred to mitochondrial proteins. Immunoblotting suggested that aging decreases an organism's ability to upregulate mitochondrial stress proteins. Compared to their young counterparts, old animals displayed a significantly delayed and blunted expression of heat shock protein 60 (Hsp60), the main inducible mitochondrial stress protein, after heat stress. Additionally, heat shock protein 10 (Hsp10) is upregulated in young, but not old, rat liver mitochondria after hyperthermic challenge. Taken together, these data suggest that mitochondria in old animals are more vulnerable to incurring and less able to repair damage that occurs in response to encountering a physiologically relevant stress. The accrual of mitochondrial damage in aged animals could lead to cellular and organ dysfunction that would have severe consequences on the survival of the organism.

ISBN: 9780549749790Subjects--Topical Terms:

1017816
Biology, Physiology.

Aging augments mitochondrial susceptibility to environmental stress.
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502 $a Thesis (Ph.D.)--The University of Iowa, 2008.
520 $a The pathophysiology of aging is accompanied by a decline in tolerance to environmental stress. While mitochondria are the primary suspects in the etiology of aging, little is known about their ability to tolerate pertubations to homoeostasis in aged organisms. To illuminate the role of mitochondria in the increased susceptibility to heat stress that is seen with aging, young (6 mo) and old (24 mo) Fischer 344 rats underwent a heat stress protocol known to elicit cellular damage that is exaggerated in aged rats. Two and 24 h after heat stress, rats were euthanized, their livers removed, and hepatic mitochondria isolated. Electron microscopy and immunoblot analysis revealed extensive structural and morphological damage to mitochondria from young and, to a greater extent, old rats. Electron paramagnetic resonance spectrometry measurements of superoxide suggested that mitochondrial integrity is also altered during heat stress. After encountering a harmful perturbation such as heat stress, the mitochondrial stress response functions to correct damage that has occurred to mitochondrial proteins. Immunoblotting suggested that aging decreases an organism's ability to upregulate mitochondrial stress proteins. Compared to their young counterparts, old animals displayed a significantly delayed and blunted expression of heat shock protein 60 (Hsp60), the main inducible mitochondrial stress protein, after heat stress. Additionally, heat shock protein 10 (Hsp10) is upregulated in young, but not old, rat liver mitochondria after hyperthermic challenge. Taken together, these data suggest that mitochondria in old animals are more vulnerable to incurring and less able to repair damage that occurs in response to encountering a physiologically relevant stress. The accrual of mitochondrial damage in aged animals could lead to cellular and organ dysfunction that would have severe consequences on the survival of the organism.
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